Abstract
The plant specific transcription factor LEAFY (LFY) plays a pivotal role in the developmental switch to floral meristem identity in Arabidopsis. Our recent study revealed that LFY additionally acts downstream of AUXIN RESPONSE FACTOR5/MONOPTEROS to promote flower primordium initiation. LFY also promotes initiation of the floral organ and floral organ identity. To further investigate the interplay between LFY and auxin during flower development, we examined the phenotypic consequence of disrupting polar auxin transport in lfy mutants by genetic means. Plants with compromised LFY activity exhibit increased sensitivity to disruption of polar auxin transport. Compromised polar auxin transport activity in the lfy mutant background resulted in formation of fewer floral organs, abnormal gynoecium development, and fused sepals. In agreement with these observations, expression of the auxin response reporter DR5rev::GFP as well as of the direct LFY target CUP-SHAPED COTYLEDON2 were altered in lfy mutant flowers. We also uncovered reduced expression of ETTIN, a regulator of gynoecium development and a direct LFY target. Our results suggest that LFY and polar auxin transport coordinately modulate flower development by regulating genes required for elaboration of the floral organs.
Highlights
The phytohormone auxin is a central regulator of lateral organ initiation [1,2,3,4]
While flowers were produced in double mutants between pin1-5 and the weak lfy-5 or lfy-6 (Ler) null mutants, they were dramatically reduced in number compared to the pin1-5 single mutant (Figure 1d,h)
These genetic interactions suggest that LFY acts synergistically with polar auxin transport to promote flower primordium initiation
Summary
The phytohormone auxin is a central regulator of lateral organ initiation [1,2,3,4]. Auxin accumulates in a graded and dynamic manner with the sites of auxin maxima correlating with the sites of primordium initiation [3,5]. NAKED PINS IN YUC MUTANT (NPY) family genes, which encode NONPHOTOTROPIC HYPOCOTYL 3-like proteins, regulate PIN endocytosis and control auxin accumulation in incipient organ primordia [11,12,13]. Plant harboring mutations in PIN1, PID, YUC, and NPY produce a few abnormal flowers [1,12,16,17] These flowers typically have fewer sepals and stamens, more petals, fused floral organs, and valveless gynoecia. We have examined the consequences of loss-of-LFY function in plants compromised in polar auxin transport by genetic means. These experiments demonstrate that LFY promotes flower primordium initiation, and subsequent floral organ initiation and development, in concert with polar auxin transport. Our study uncovers a complex set of interactions between LFY and the auxin pathway in flower development
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